Objective To compare the effects of vagus nerve electrical stimulation postconditioning with limb remote ischemic postconditioning on inflammatory response during myocardial ischemia reperfusion in rat in vivo. Methods Eighty male Sprague-Dawley rats weighing 290-320 g were randomly allocated into four groups (n=20 in each group): sham group (S group); ischemia reperfusion group (I/R group); postconditioning with vagus nerve electrical stimulation group (POES group) and limb remote ischemic postconditioning group (LRIPOC group). In the groups other than the sham group, the myocardial ischemia reperfusion model was preparated by ligation of left anterior descending coronary artery for 30 min, followed by 120 min of reperfusion. During process of ischemia and reperfusion, HR and MAP were recorded and the rate pressure product (RPP) at every measuring point was calculated as the index of myocardial oxygen consumption. In ten rats randomly selected from each group, the blood samples were collected from carotid artery at 30 min, 60 min and 120 min after reperfusion. Then, serum concentrations of cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), tumor necrosis factor α (TNF-α), high mobility group box-1 protein (HMGB-1), intercellular adhension molecule 1 (ICAM-1), interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-10 (IL-10) were assessed using enzyme-linked immunosorbent assay (ELISA) kits. At the end of experiment, the infarct volumes were assessed by Evans blue and triphenyltetrazolium chloride (TTC) staining. In another ten rats randomly selected from each group, the myocardial contents of TNF-α, HMGB-1, ICAM-1, IL-1, IL-6 and IL-10 in ischemic and non-ischemic regions were measured with ELISA kits after the rats were euthanized. Results Compared to the baseline value, the HR at 15 min of myocardial ischemia in POES group was significantly decreased. And the MAP and RPP at onset of myocardial ischemia were significantly lower in I/R, POES and LRIPOC groups than those in the S group. Compared to the sham group, the infarct volume, serum concentrations of cTnI and CK-MB, serum concentrations of TNF-α at 30 min, 60 min and 120 min after reperfusion, serum concentrations of HMGB-1 at 60 min and 120 min after reperfusion, serum concentrations of ICAM-1, IL-1 and IL-6 at 120 min after reperfusion, myocardial concentrations of TNF-α, HMGB-1, ICAM-1, IL-1, IL-6 and IL-10 in both ischemic and non-ischemic regions increased significantly in the I/R group. The infarct volume, serum concentrations of cTnI and CK-MB, serum concentration of TNF-α at 30 min and 60 min after reperfusion, levels of TNF-α, HMGB-1, ICAM-1, IL-1 and IL-6 in serums and myocardia (ischemic and non-ischemic regions) were all significantly lower in both POES and LRIPOC groups than those in the I/R group. However, compared to the I/R group, the myocardial content of IL-10 in both ischemic and non-ischemic regions significantly increased in the POES group. As compared to the POES group, the infarct volume, serum concentration of cTnI, serum concentration of TNF-α at 60 min after reperfusion, serum concentrations of HMGB-1, ICAM-1, IL-1 and IL-6 at 120 min after reperfusion, myocardial contents of ICAM-1, IL-1 and IL-6 in ischemic region, myocardial contents of HMGB-1, ICAM-1, IL-1 and IL-6 in non-ischemic region were all significantly increased in the LRIPOC group, but the myocardial content of IL-10 in ischemic region was significantly lower in LRIPOC group than that in the POES group. Conclusions The inflammation inhibiting effect of POES is stronger than that of LRIPOC during myocardial ischemia reperfusion injury, which may be one of reasons why the POES can provide a more powerful protection against myocardial ischemia reperfusion injury than the LRIPOC.